Hemodynamic disorders 2.pdf

EDEMA  Edema: is increase f luid in interstitial space (collection in body cavities called hydrothorax o, hydropericardium and hydroperitoneum (ascites). Pathophysiology of edema:  Vascular hydrostatic pressure &plasma colloid osmotic pressure control the movement of f luid between vascu...

EDEMA  Edema: is increase f luid in interstitial space (collection in body cavities called hydrothorax o, hydropericardium and hydroperitoneum (ascites). Pathophysiology of edema:  Vascular hydrostatic pressure &plasma colloid osmotic pressure control the movement of f luid between vascular & interstitial spaces.  The outf low of f luid from arteriolar end is balanced by the inf low at the venular end and small amount drain by lymphatics.  To thoracic duct and eventually to left subclavian vein Increased interstitial Hydrostatic pressure fluid pressure Arterial end CAPILLARY BED Venous end  Factors regulate edema:  1- Increase capillary hydrostatic pressure or decrease colloid osmotic pressure.  2- Effect of inf lammatory mediators on vascular permeability.  3- Lymphatic obstruction can impair f luid drainage &cause edema.  Edematous f luid in hydrodynamic disturbances is transudates with specific gravity 1.012 while inf lammatory edema due to increased vascular permeability is exudates (1.020).  Increased hydrostatic pressure: Regional increases in hydrostatic pressure can result from a focal impairment in venous return e.g (deep venous thrombosis DVT) with edema of the affected limb.  Generalized increase in venous pressure leading to systemic edema occur in congestive heart failure in which reduced cardiac output causes reduced renal perfusion & trigger of rennin angiotensin aldosterone axis causing sodium & water retention by kidney in order to increase intravascularvolume & improve cardiac output & renal perfusion.  This extra f luid load only increased venous pressure & edema.Unless cardiac output restored or renal f luid retention reduced (e.g salt restriction , diuretics &/or aldosteron antagonists),vicious cycle of renal f luid retention & worsening edema result. Mechanism of edema formation in heart failure , renal failure and hepatic failure Reduced plasma osmotic pressure: (reduced plasma proteins)  Result from: Increased loss of albumin as in nephrotic syndrome. Reduced protein synthesis as in cirrhosis, malnutrition. Protein losing enteropathy(intestinal diseases with malabsorption) Lymphatic obstruction: Usually localized:  Causes: 1. Inf lammatory obstruction e.g filariasis which causes lymphatic obstruction& lymph node fibrosis in inguinal region leading to edema of genitalia& lower limb (elephantiasis). 2. post surgical or post-irradiation : Cancer of breast treated by surgery or irradiation with resection of lymphatic drainage of upper limb & scarring; there is edema of the arm. 3. Neoplastic : In CA breast, infiltration & obstruction of superficial lymphatics will cause edema of breast skin (peau-de-orange) due to accentuation of depression in the skin at site of hair follicles.  Peau d'orange and post-mastectomy lymphedema Morphology of edema:  Microscopically: Clearing & separation of extra cellular matrix.  Any organ or tissue can be involved, but edema is most commonly seen in subcutaneous tissues, the lungs, and the brain  In most cases the distribution is inf luenced by gravity and is termed dependent edema (e.g., the legs when standing, the sacrum when recumbent). Finger pressure over substantially edematous subcutaneous tissue displaces the interstitial f luid and leaves a depression, a sign called pitting edema Special forms of edema: 1. Pulmonary edema Seen in: 1. Left sided heart failure (dependent distribution in lung) 2. Respiratory distress syndrome. 3. Pulmonary infection. 4. Hypersensitivity reaction.  The lung is 2-3 times their normal weight, cut section frothy, blood tinged f luid represent mixture of air, edematous f luid & extravasated RBCs. 2. Edema of brain  Localized: due to abscess, neoplasm &trauma.  Generalized: due to encephalitis, hypertension crises, venous outf low obstruction &trauma  Grossly: Swollen with narrowed sulci & distended gyri. Clinical correlation of edema:  a. Subcutaneous edema in cardiac failure & renal failure can impair wound healing or clearance of infection.  b. Pulmonary edema can cause death by interfering with normal ventilatory function by:  (1) f luid collects in alveolar space& impair oxygen diffusion).  (2)Edematous f luid in alveolar spaces is favorable environment for bacterial infection. Clinical consequnces of edema-continue  c. Brain edema if severe causes death due to brain herniated through foramen magnum which causes compression of vital centers & also due to compression of vascular supply of brain.  Hyperemia & Congestion Hyperemia and congestion both stem from locally increased blood volumes  Hyperemia is an active process in which arteriolar dilation (e.g., at sites of inf lammation or in skeletal muscle during exercise) leads to increased blood f low  Affected tissues turn red (erythema) because of the engorgement of vessels with oxygenated blood.  Hyperemia could be : 1. Local or General 2. Physiological or Pathological  Localized hyperemia: could be A. physiological: e.g f lushing, exercise, after meal. B. Pathological : e.g site of inf lammation.  Generalized hyperemia: could be A. Physiological : e.g hot weather. B. Pathological: e.g:  Fever, Hyperthyroidism, Arteriovenous shunt  *Congestion: is passive process from impair outf low from tissue (venous obstruction).  Congested tissues take on a dusky reddish-blue color (cyanosis) due to red cell stasis and the accumulation of deoxygenated hemoglobin.  As a result of the increased volumes and pressures, congestion commonly leads to edema.  long-standing chronic passive congestion, the lack of blood f low causes chronic hypoxia  Capillary rupture in chronic congestion can also cause small hemorrhagic foci; subsequent catabolism of extravasated red cells can leave residual clusters of hemosiderin-laden macrophages.  1- Generalized systemic congestion e.g right ventricular failure in which there is decrease venous return to the heart with accumulation of blood in the venous side.  Clinically:  A- Dilated veins e.g increase JVP (jugular venous pressure)  B- Edema (limbs, ascites, hepatospleenomegaly).  Morphology of generalized congestion:  Liver: will show chronic venous congestion causing a grossly mottled appearance similar to the nut meg hence the name Nut meg liver.  Mic.:  Congestion of the central venule.  Necrosis of the surrounding hepatocytes because of pressure &hypoxia.  The peripheral liver cells are normal or show fatty change. Liver with chronic passive congestion and hemorrhagic necrosis  2- Pulmonary venous congestion: e.g left ventricular failure where there is accumulation of blood in the surrounding capillaries, RBCs will escape to the alveolar space & engulfed by macrophages (heart failure cells) which cause cough with blood stained sputum.  3- Localized venous congestion: e.g DVT of leg (edema, cold, cyanosis). HEMORRHAGE  Is extravasation of blood into the extravascular space  It is either external or internal (encased within tissue( hematoma) which may be: Insignificant (bruises) or Massive (retroperitoneal hematoma) from rupture of dissecting aortic aneurysm &cause death.  Petechiae: Minute hemorrhage in skin ,mucous membranes & serosal surfaces(1-2 mm)  Slightly larger (≥3 mm) hemorrhages are called purpura.  Ecchymosis: 1-2 cm subcutaneous hematoma  Causes of Hemorrhage: 1. Trauma: e.g penetrating wounds to the heart & large vessels----- rapid blood loss. 2. Abnormalities of blood vessel wall like: Inf lammatory lesions may lead to weakening of arteries &may cause aneurysmal dilatation &rupture. Neoplastic invasion e.g. carcinoma of tongue with invasion of lingual arteries. Other vascular diseases e.g atheroma, aneurysm.  3- High pressure within blood vessel e.g systemic HT leading to hemorrhage at sites of arterial weakness or increase venous pressure in varicose veins e.g. legs ,esophageal hemorrhage.  Effects of acute hemorrhage:  Depend on volume &rate of blood loss: as following  a. the effect is slight if less than 20% of blood volume is lost, while sudden loss of 33% of blood volume leads to death.  b. Gradual loss (within 24 hour) of more than 50% blood volume is not necessarily fatal but it is serious.  C. chronic blood loss can lead to iron-deficiency anemia  In human 60-70% of blood volume contained in veins &venules, so constriction of these vessels will increase venous return to the heart.  Arteriolar constriction is selective i.e there is decrease blood f low to skin, salivary glands, liver, spleen & kidneys while blood is preserved to the brain, heart, skeletal muscles &diaphragm. Shock:  It is a state in which the supply of blood to the tissues is inadequate to meet the metabolic demands  is characterized by systemic hypotension due either to reduced cardiac output or to reduced effective circulating blood volume Classification:  1- Hypovolemic shock: In which there is a real decrease in blood volume.  Causes: Hemorrhage. Fluid loss as in severe vomiting, diarrhea & burns.  Mechanism of development: is inadequate blood or plasma volume with resultant low cardiac output  2- Cardiogenic shock: There is relative decrease in blood volume (pooling of blood).  Causes: ❖ Myocardial infarction. ❖ Rupture of the heart. ❖ Pulmonary embolism. ❖ Arrhythmias. ❖ Cardiac temponade. Mechanism of development: Failure of myocardial pump due to intrinsic myocardial damage or extrinsic pressure or obstruction to outf low with reduced output  3- Septic shock: Causes: ❖Overwhelming bacterial infection by gram positive or (gram negative septicemia or endotoxic shock) or fungi ❖Septic shock is associated with severe hemodynamic and hemostatic derangements, With a mortality rate near 20% Pathogenesis of septic shock 1. Role of inf lammatory mediators: Various microbial cell wall constituents engage receptors on inf lammatory cells with extensive release of mediators that activate endothelial cells and coagulation system → procoagulant state 2. Role of endothelial cells: injury results in (1) Thrombosis –> DIC in half of patients (2) increased vascular permeability→ edema (3) vasodilation , through release of vasoactive substances → pooling of blood 3. Metabolic abnormalities. Septic patients exhibit insulin resistance and hyperglycemia( increase stress hormones) later in the course adrenal insufficiency 4. Organ dysfunction. Systemic hypotension, interstitial edema, and small vessel thrombosis all decrease the delivery of oxygen and nutrients to the tissues  4- Neurogenic shock:  Causes: Anesthesia & spinal cord injury. o Mechanism: peripheral vasodilatation due to loss of vascular tone Stages of shock:  1- Non progressive phase: which is the compensatory phase.In this stage a compensatory mechanisms operate to maintain cardiac output &blood pressure near normal levels.The compensatory mechanisms include:  a- Arteriolar constriction leading to increase blood pressure.  b- Increase heart rate &cardiac output.  c- Retention of f luid through increase secretion of ADH & activation of rennin angiotensin aldosteron axis to retain f luid.  2- Progressive phase :When an additional factor is added like extensive burn complicated by bacterial infection.  In this stage ,despite the compensatory mechanisms ,there is progressive decline in blood pressure &cardiac output.  Clinically observed as increase in respiratory rate &decrease in urine output ref lecting pulmonary &renal hypoperfusion.  3. Irreversible Phase: result from irreversible injury to the cell membrane as manifested by dysfunction of sodium-potassium pump & defect in cell membrane so cell contents go to outside.  The reduction in blood f low to the vital organs such as brain, heart, kidney lead to ischemic cell death in these organs. Clinical course:  In hypovolemic &cardiogenic shock: patient present with hypotension, weak rapid pulse, tachypnea, cool &cyanotic skin.  In septic shock: the skin may initially be warm &f lushed because of peripheral vasodilatation. Prognosis:  In hypovolemic shock: 80-90% of young patients survive.  Cardiogenic shock associated with extensive myocardial infarction & in gram-negative shock, 75% died. Thank you